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198 S. Ghosh et al. / Mutation Research 723 (2011) 190–198 ture for activation of apoptotic responses. Further studies in this direction will reveal the importance of such response. The use of oxygen beam therapy has definite advantage over gamma therapy and the understanding of the mechanism of apoptosis will give the clinician a handle to manipulate therapy for enhanced cell killing. Conflict of interest The authors declare that there are no conflicts of interest. Acknowledgements This work was funded by Board of Research in Nuclear Sciences, Department of Atomic Energy [DAE], Government of India, through a project sanctioned to one of the authors, AS, bearing sanction number 2007/37/37/BRNS. All the authors are thankful to the Director, IUAC, New Delhi for providing radiation facility for the work. We would also like to extend our thanks to all the members of Pelletron group of IUAC for their sincere help during irradiation. 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Cancer Investigation, 28:615–622, 2010 ISSN: 0735-7907 print / 1532-4192 online Copyright c○ Informa Healthcare USA, Inc. DOI: 10.3109/07357901003630991 ORIGINAL ARTICLE Cellular and Molecular Biology Low Energy Proton Beam Induces Efficient Cell Killing in A549 Lung Adenocarcinoma Cells Somnath Ghosh, 1 Nagesh N. Bhat, 2 S. Santra, 3 R. G. Thomas, 3 S.K. Gupta, 3 R.K. Choudhury, 3 and Malini Krishna 1 Radiation Biology and Health Sciences Division, 1 Radiological Physics and Advisory Division, 2 Nuclear Physics Division, Bhabha Atomic Research Centre, Trombay, Mumbai, India 3 Cancer Invest Downloaded from informahealthcare.com by University of Chicago Library on 06/10/11 For personal use only. ABSTRACT The aim of the current study was to determine the signaling differences between γ- and proton beam-irradiations. A549 lung adenocarcinoma cells were irradiated with 2 Gy proton beam or γ-radiation. Proton beam was found to be more cytotoxic than γ-radiation. Proton beam-irradiated cells showed phosphorylation of H2AX, ATM, Chk2, and p53. The mechanism of excessive cell killing in proton beam-irradiated cells was found to be upregulation of Bax and downregulation of Bcl-2. The noteworthy finding of this study is the biphasic activation of the sensor proteins, ATM, and DNA-PK and no activation of ATR by proton irradiation. INTRODUCTION Exposureof mammalian cells to ionizing radiation leads to the activation of several signaling pathways that result in apoptosis. Although, the end point, apoptosis is effectively activated by conventional X-ray treatment, the development of radioresistance following therapy remains a major cause for concern. Clinicians are now favoring proton beam therapy to avoid the issue (1–6). However, the mechanism of cell killing by proton beam is not yet well delineated. Lung cancer is a frequently occurring, mostly lethal disease in all countries worldwide (7). It is one of the most commonly diagnosed types of cancer and has the highest death rate (8, 9). Overall, fewer than 10% of people with primary lung cancer are alive 5 years after diagnosis. Depending on tumor size, location, and histology, several treatment options are available, including surgery and radiotherapy (RT), both often combined with chemotherapy (10). A major problem remains local tumor control (11, 12). Therefore, new ways to deliver radiotherapy beyond photons have been sought for, including protons (13, 14) Keywords Proton beam, ATM, p53, Bax, Bcl-2 Correspondence to: Malini Krishna Radiation Biology and Health Sciences Division Bhabha Atomic Research Centre Trombay, Mumbai India, 400085 email: malini@barc.gov.in; malinik00@gmail.com and carbon ions (15). Furthermore, treatment with charged particle radiation has several potential advantages over treatment with γ or X-ray radiation such as the Bragg peak enables precise localization of the radiation dose, an inverted depth-dose distribution, a higher relative biological effectiveness (RBE), and a lower cellular capability for repair of radiation injury. Because of their superior dose distribution, a therapeutic gain can be expected with charged particles (1–4). Although proton beams are currently being used for the treatment of many cancers (1–6), the mechanism of cell killing and its variance from γ -irradiation is not well understood. Understanding the specific biological effects of charged particle radiation on cancer cells could also provide valuable insights for the design of novel therapeutic applications for the treatment of cancers, which are resistant to many types of therapies. Moreover, therapies can be designed only if the signaling pathway is understood. A cytological manifestation of nuclear activity in response to ionizing radiation (IR) is the formation of the socalled IR-induced foci (IRIF) (16). IRIFs are dynamic, microscopically discernible structures containing thousands of copies of proteins, including γ H2AX, ataxia telangiectasia mutated (ATM), BRCA1, 53BP1, MDC1, RAD51, and the MRE11/RAD50/NBS1 (MRN) complex, which accumulate in the vicinity of a DNA double-strand breaks (DSB) (17, 18). It is being appreciated lately that DNA repair pathways activated by charged particle radiation might be different from those studied after γ -irradiation. When exposed to ionizing radiation, eukaryotic cells also activate checkpoint pathways to delay the progression of the 615
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RADIATION INDUCED SIGNALING IN MAMM
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DECLARATION I, hereby declare that
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CONTENTS Page No. SYNOPSIS………
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2.11 Measurement of NO production
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PREAMBLE SYNOPSIS Ionising radiatio
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SYNOPSIS Aims and Objectives: To St
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SYNOPSIS 2.6 Immunofluorescence sta
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SYNOPSIS ATM gene expression, which
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SYNOPSIS Percentage Survival 100 80
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SYNOPSIS Ratio of Rad52 to Actin Ra
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Relative Phosphorylation 45 40 35 3
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SYNOPSIS Fig. 3.3A Clonogenic Cell
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SYNOPSIS (A) Av No. of phospho BRCA
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SYNOPSIS Percentage Survival 120 10
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SYNOPSIS Fig.3.4B. Existance of cro
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SYNOPSIS Fig. 3.4EDNA damage in EL-
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SYNOPSIS subsequent cytotoxicity ca
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SYNOPSIS [4] Hall, E. J. Radiobiolo
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CHAPTER 1 INTRODUCTION INTRODUCTION
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CHAPTER 1 INTRODUCTION 15.8% 9.56%
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CHAPTER 1 INTRODUCTION far apart an
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CHAPTER 1 INTRODUCTION and are more
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CHAPTER 1 INTRODUCTION 1.3 DNA dama
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CHAPTER 1 INTRODUCTION associates w
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CHAPTER 1 INTRODUCTION are unable t
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CHAPTER 1 INTRODUCTION Perhaps one
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CHAPTER 1 INTRODUCTION occurs at DS
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CHAPTER 1 INTRODUCTION related prot
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CHAPTER 1 INTRODUCTION damage must
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CHAPTER 1 INTRODUCTION At the prese
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CHAPTER 1 INTRODUCTION predominant
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CHAPTER 1 INTRODUCTION provide a me
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CHAPTER 1 INTRODUCTION hypersensiti
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CHAPTER 1 INTRODUCTION cycle-specif
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CHAPTER 1 INTRODUCTION 1.4 Overview
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CHAPTER 1 INTRODUCTION 1.4.1 Radiat
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CHAPTER 1 INTRODUCTION interaction
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CHAPTER 1 INTRODUCTION p90S6 kinase
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CHAPTER 1 INTRODUCTION CD4 (formerl
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CHAPTER 1 INTRODUCTION unrepaired d
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CHAPTER 1 INTRODUCTION well to the
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CHAPTER 1 INTRODUCTION 1.6 Radiatio
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CHAPTER 1 INTRODUCTION becomes pote
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CHAPTER 2 MATERIALS AND METHODS MAT
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CHAPTER 2 MATERIALS AND METHODS 2.2
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CHAPTER 2 MATERIALS AND METHODS res
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CHAPTER 2 MATERIALS AND METHODS Arr
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CHAPTER 2 MATERIALS AND METHODS PBS
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CHAPTER 2 MATERIALS AND METHODS the
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CHAPTER 2 MATERIALS AND METHODS 2.1
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CHAPTER 3 RESULTS RESULTS 93
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CHAPTER 3 RESULTS fractionated regi
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CHAPTER 3 RESULTS On comparison of
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CHAPTER 3 RESULTS Table 3.1.2A List
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CHAPTER 3 RESULTS 80 NM_002185 IL7R
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CHAPTER 3 RESULTS SAA2 149 AU134977
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CHAPTER 3 RESULTS 221 LOC643167 RNA
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CHAPTER 3 RESULTS 299 BF244402 FBXO
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CHAPTER 3 RESULTS CDK4) 57 AU152107
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CHAPTER 3 RESULTS 134 AL045793 METT
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CHAPTER 3 RESULTS 58 AF237813 ABAT
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CHAPTER 3 RESULTS 127 AI809749 ORMD
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CHAPTER 3 RESULTS 31 BE615699 UNC84
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CHAPTER 3 RESULTS 47 AF026303 SULT1
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CHAPTER 3 RESULTS 117 BF062193 CYor
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CHAPTER 3 RESULTS 187 AL036662 ---
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CHAPTER 3 RESULTS 52 AV686514 EMP2
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CHAPTER 3 RESULTS exposed to 10 Gy
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CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
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CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
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CHAPTER 3 RESULTS Fig. 3.1.7 Transl
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CHAPTER 3 RESULTS 3.1.9 Stabilizati
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CHAPTER 3 RESULTS 23±1.5% (Fig. 3.
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CHAPTER 3 RESULTS whereas only the
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CHAPTER 3 RESULTS with equal doses
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CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
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CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
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CHAPTER 3 RESULTS (7.5±0.64) (Fig.
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CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
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CHAPTER 3 RESULTS 3.3.2 Oxygen beam
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CHAPTER 3 RESULTS in all the cells.
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CHAPTER 3 RESULTS 3.3.2.3 Radiation
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CHAPTER 3 RESULTS Fig.3.3.2.7 Apopt
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CHAPTER 3 RESULTS PMA stimulated U9
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CHAPTER 3 RESULTS Fig.3.4.2. Exista
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CHAPTER 3 RESULTS up-regulation of
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CHAPTER 3 RESULTS Fig.3.4.3.2 NO pr
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CHAPTER 3 RESULTS 3.4.3.4 Apoptotic
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CHAPTER 3 RESULTS 3.4.4 Bystander e
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CHAPTER 3 RESULTS Fig.3.4.4b DNA da
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CHAPTER 3 RESULTS Fig.3.4.5a Gene e
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CHAPTER 4 DISCUSSION DISCUSSION 185
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CHAPTER 4 DISCUSSION directly expos
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CHAPTER 4 DISCUSSION dose is delive
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CHAPTER 4 DISCUSSION A clear cause
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CHAPTER 4 DISCUSSION 4.2 Proton bea
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CHAPTER 4 DISCUSSION Although the e
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CHAPTER 4 DISCUSSION Similar number
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CHAPTER 4 DISCUSSION the mechanism
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CHAPTER 4 DISCUSSION Thus unlike th
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CHAPTER 4 DISCUSSION different from
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CHAPTER 4 DISCUSSION upregulates ma
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CHAPTER 4 DISCUSSION Numerous studi
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CHAPTER 4 DISCUSSION inhibition of
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CHAPTER 4 DISCUSSION The survival o
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CHAPTER 5 REFERENCES [1] Khan, F. T
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CHAPTER 5 REFERENCES [19] Woo, R. A
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CHAPTER 5 REFERENCES [35] Nghiem, P
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CHAPTER 5 REFERENCES [52] McKay, B.
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CHAPTER 5 REFERENCES [69] Cary, R.
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CHAPTER 5 REFERENCES [84] Uziel, T.
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CHAPTER 5 REFERENCES [98] Liu, Y.;
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CHAPTER 5 REFERENCES [111] Fei, P.;
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CHAPTER 5 REFERENCES [127] Frank, K
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CHAPTER 5 REFERENCES [141] Pierce,
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CHAPTER 5 REFERENCES [156] Roots, R
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